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Bacteriology > Bacterial Toxins and Anaerobes > Flashcards

Bacterial Toxins and Anaerobes Flashcards

1
Q

4 properties of a successful pathogen

A
  1. Gain access into host: correct portal of entry
  2. Colonize host tissue: Attachment to specific host tissue
  3. Resist host-defense mechanism: Non-specific (TLR and cytokines and macrophage) or specific (Aquired T and B cell mediated)
  4. Damage host: Pathogens
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2
Q

two mechanisms of pathogenicity

A
  1. Invasiveness: ability to enter host (and replicate in it)

2. Toxigenicity (ability to produce a toxin)

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3
Q

Where is anaerobic bacteria usually located

A

hundred of species of anaerobes on mucosal surfaces

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4
Q

How many anaerobic species are important in human pathogens

A

only a few

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5
Q

Describe the composition of infection by anaerobes

A

mixed, opportunistic infections. Include either/both aerobic or anaerobic bacteria

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6
Q

Describe how anaerobes are sensitive to O2 intermediates

A
  • they have little superoxide dismutase to remove O2 radicals
  • they have low amounts of catalase to remove H2O2
  • they often lack cytochromes so usually metabolize via fermentation
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7
Q

Site of infections for anaerobic gram negative pathogens

A

colon ( intra-abdominal abscess) mouth and skin

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8
Q

infections by anaerobic gram negative pathogens are often foul smelling-why?

A

due to short chain fatty acids produced during fermentations

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9
Q

anaerobic gram negative pathogens do fermentation metabolism and therefore are often

A

gas producing

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10
Q

Describe the Poly-microbial nature of the anaerobic infection

A

infections often due to the contamination of tissue by

normal flora

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11
Q

How do you isolate isolate anaerobic pathogens

A

culture techniques

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12
Q

anaerobic gram negative pathogens are often void of pathogens

A

aerobic bacteria (anoxic environment)

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13
Q

Common gram negativ anaerobic pathogen

A

Bacteriodes fragilis

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14
Q

Most intra-abdominal infections are due to

A

Bacteriodes fragilis

-common inhbaitant of bowel

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15
Q

Virulence factor for Bacteriodes fragilis

A

-polysaccharide capsule (anti-phagocytic)
-Bacteroides are aerotolerant anaerobes able to tolerate
atmospheric concentrations of oxygen.
-Bacteroides encode two major oxidative stress
response genes, catalase and superoxide dismutase.

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16
Q

•B. fragilis often isolated in mixed bacterial infection with;

A
  • other anaerobes

- with facultative anaerobes (often Peptostreptococcus (gram positive anaerobic cocci) in intra-abdominal abscess

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17
Q

Describe the structure of Bacteriodes fragilis

A

pleomorphic often bacilli

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18
Q

What should you grow bacteria in if you want to see if it is Bacteriodes fragilis

A

bile salts ans gentamicin

most aerobic and anaerobic bacteria are inhibited by bile salts and gentamicinexcept for Bacteriodes fragilis.

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19
Q

While Bacteriodes fragilis are the most intra-abdominal infections, the types of pathogens isolated in other surgical sites differ:

A
  • sites of infection are pathogen-specific

- mixed infections are common

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20
Q

Surgical site infections in cardiac surgery patients

A

gram-positive organisms 48%

gram negative organisms 40%

fungi 12%

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21
Q

Clostridia

A

Anaerobic gram positive, spore forming bacili

obligate anaerobes or aerotolerant

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22
Q

Pathogenesis of clostridia

A

-due invasiveness or an exotoxin

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23
Q

Physiology of clostridia

A

either saccharolytic – sugars
or
proteolytic – amino acid

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24
Q

Where doe sclostridia live

A

soil inhabitant or inhabitant of intestinal tract

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25
Q

Invasive clostridia

A

histotoxic: C. perfringens

produces alpha toxin (pholpholipase) causes tissue damage

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26
Q

Toxin producing clostridia: gastrointestinal disease:

A

C. difficile (Toxin A and Toxin B)

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27
Q

Toxin producing clostridia: tetanus:

A

C. tetani, (tetanus toxin)

28
Q

Toxin producing clostridia : botulism, food poisoning:

A

C. bolulinum, botulinum toxin

29
Q

Histotoxic clostridia

A

-invasive and cause extensive destruction of muscle and connective tissue
-characterized by the formation of gas.
-Invasive C. perfringens (alpha toxin):-cause most clostridial-mediated
myonecrosis
-pathology: A deep wound to muscle predisposes infection
-gas gangrene

30
Q

Steps of infection by C. perfringens (alpha toxin)

A
  • reduction of tissue redox potential leading to host cell death. It turns pyruvate into lactate which decreases the pH
  • host proteases release the nutrient from the host tissues and the clostridia grow
  • C. perfringens releases an alpha toxin which is a phospholipase and cases tissue damage
31
Q

C. perfringens toxin

A

alpha toxin. It is a phospholipase and causes tissue damage

32
Q

What does a C. perfringens infection cause adn how do you treat it

A

gas gangrene- treatment is antibiotic and often excision with amputation

33
Q

4 types of bacterial infection

A
  1. surface acting toxin
  2. pore forming toxin
  3. A/B toxin (extreme potency)
  4. Type II and IV toxin (injects it toxin and produces 100os of molecules to inject into host and paralyze neutrophils) (Mortal Combat)
34
Q

Each bacterial toxin has what two components

A

catalytic component and a host cell binding component

35
Q

Catalytic component of bacterial toxin

A

modifies specific host macromolecules (post-translational modification)

36
Q

Host cell binding component

A

may be tissue specific (clostridial neurotoxin) or not tissue specific ( diptheria toxin)

37
Q

Diphtheria toxin and Pseudomonas aeruginosa exotoxin A

A

ADP-ribosylate EF2(elongation factor 2 of the host) : inhibits proteins synthesis

38
Q

Botulinum toxin & Tetanus toxin:

A

Protease for SNARE proteins: inhibits neurotransmittor vesicle fusion to the cell membrane

39
Q

Large Clostridium difficile toxins:

A

Glucosylate Rho proteins: inhibits cell motility and

ultrastructure, via active modification

40
Q

Shiga toxin:

A
  • a little unusual bc although it is a protein toxin its targets RNA
  • Deadenylates a adenine on RNA: inhibits protein synthesis
41
Q

How do we vaccinate for bacteria that produce toxins

A

lot of times we use an inactive component of their toxin called a toxoid

42
Q

DT/ TT vaccine

A

formalin inactivated diphtheria/tetanus toxins

43
Q

Conjugate vaccines

A

Hib polysaccharide conjugated to diphtheria
toxoid, making a T cell-dependent immune response (IgM IgG
and memory)

44
Q

Antibiotic-associated diarrhea (gastrointestinal colitis) Causative agent: and what toxins does it produce

A

C. difficile
A and B toxins

because
AB CD

Antibiotic therapies may be associated with C. difficile infections where the normal floral are reduced allowing endogenous and ingested C. difficile to expand and produce Toxin A and Toxin B, which contribute to diarrhea and inflammation.

C. difficile infection range from asymptomatic to recurrent and life-
threatening

45
Q

Pathology of clostridium difficile

A

C. difficle produces Toxin A and Toxin B which glucosylate Rho
GTPases elicit:

actin depolymerizationdisrupt gut epithelial cells diarrhea

UDP-glucose + Rho  Rho-glucose (inactive) + UDP

46
Q

Whats going on in Canada . with C. difficile

A

Emergence of a highly toxic strain of C. difficile that is resistant to fluoroquinolones has caused outbreaks in the US and Canada.

47
Q

What produces the most toxic protein for humans

A

Clostridia

48
Q

C. botulinum symptoms

is there a vaccine

A
  • flaccid paralysis

- no vaccine

49
Q

C. tetani
symptoms
is there a vaccine

A
  • spastic paralysis (lock jaw)

- licensed vaccine

50
Q

WHy is it difficult to produce a vaccine for Botulinum toxin

A

there are seven serotypes A,B,C,D,E,F,G defined by antiser neutralization

an effective vaccine would have to protect against all seven serotypes and that would be hard to do

51
Q

Mechanism of Action of Clostridium neutotoxins

A
  • proteases
  • BoNT and TeNT have the same mechanism of action (cleave SNARE proteins)
  • cleaves SNARE proteins to inhibit synaptic vesicle function
  • they have the exact same catalytic activity and even cleave at the same site but they have different physiologies bc the SNARE toxin does not define the spasticity of each toxin
52
Q

If the cleavage of the SNARE protein is not responsible for the pathologies what is

A
  • intracellular trafficking
  • BoNT remains in the periphery (synaptic vesicles)
  • TeNT (retrograde traffice to CNS)
53
Q

BoNT pathology is caused by

A

peripheral action at the motor neuron, yielding an inhibition of acetyl choline release at the neuromuscular junction (flaccid paralysis)

54
Q

Tetanus toxin pathology is caused by

A

retrograde trafficking to inhibitory interneuron, stimulates acetyl choline release at the neuromuscular junction (spastic paralysis)

55
Q

tetanus, C. tetani physiology

A

• Anaerobe
• Proteolytic (peptides & amino acids)
• Tetanus toxin responsible for the clinical
symptoms of tetanus

56
Q

Determinants of Pathogenicity for C tetani

A

C. tetani is not invasive, remains at site of infection,

but produces tetanus toxin

57
Q

Intoxication

of C. tetani

A

– Following injury with a mixed bacterial infection
– soil bacteria ferment to reduce redox potential
– allows limited growth of C. tetani, sufficient for toxin
production

58
Q

How do we prevent tetanus infection

A

immunization

the preventative vaccine is made from tetanus toxin that was treated with formalin to be tetanus toxoid

59
Q

Preventative vaccine

A

There is a vaccine to prevent tetanus, diptheria, and pertussis DTaP, Tdap, DT, Td

60
Q

At what age is the DTaP vaccine given and why

A

5 doses given at 2, 4, 6, and 15-18 months and 4-6 years.

It is given at 2 months bc that is when you lose protection from maternal antibodies

61
Q

Therapeutic vaccine

A

treatment in a suspected case of tetanus

62
Q

Botulism is caused by

A

Clostridium botulinum

63
Q

Botulism: Clostridium botulinum Pathogenicity

A

– Botulinum toxin: AB toxin
– Zinc Protease (heat labile)
– inhibits neurotransmitter release: flaccid paralysis

64
Q

Seven BoNT serotypes (A, B, C, D, E, F, and G)

A

– Each serotype is defined by the absence of cross neutralization
by serotype specific antisera
*• For example, anti-BT/A antisera neutralizes only BT/A

BoNT serotypes A, B, E, and F most common natural forms for
humans

-so there is no licensed vaccine bc there are so many serotypes

65
Q

Why is BoNT a potent human therapy for neurological diseases

A

-depending on the serotype it can last for up to 5 months!!!

  • not contagious
  • not trasnmitted from person to person
  • neuronal specificity
66
Q

BoNTs are clinically useful due to neuron specificity…explain

A
  • Bind receptors on neurons
  • cleave neuronal SNARE substrates
  • therefore limited off targets…super specific!!
67
Q

Most common use of BoNT for therapy

A

for bleopharospasm-absnormal contraction or twitch of eyelid neurons (functional blindness)

  • BoNT cleaves the SNARE proteins in the spastic nerves relieving spasticity
  • BoNT has a long half life in nerons (months long therapy per injection0

Bacteriology (15 decks)

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